Proteomics

Dataset Information

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Investigation of hepatic stellate cell proteomics during activa-tion with fetal bovine serum


ABSTRACT: Hepatic stellate cells (HSCs) are the major driving factor in liver fibrosis. Upon liver inflammation caused by alcohol abuse and/or a fatty liver, HSCs transform from a quiescent- into a proliferating, fibrotic phenotype. We study this transformation termed “activation”, using state of the art TIMS-TOF mass spectrometry proteomics, as well as phenotype analysis of the immortalized LX-2 HSC cell line. In our work we employ a simple, yet reliable model of HSC activation via an in-crease in growth media serum concentration (serum activation). Protein network analysis of ac-tivated LX 2 cells reveals an increase in the production of ribosomal proteins and proteins related to migration. Interestingly, we could also observe a decrease in the expression of lipogenic pro-teins and a loss of cytosolic lipid droplets during activation. Especially the downregulation of proteins associated with cholesterol biosynthesis might be a promising target for further study. This work provides an update on HSC activation characteristics using contemporary proteomic and bioinformatic analysis and presents an accessible model for HSC activation.

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell

SUBMITTER: Maximilian Schinagl  

LAB HEAD: Ruth Birner-Gruenberger

PROVIDER: PXD029121 | Pride | 2022-02-14

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
LX2_FBS_treatment.zip Other
checksum.txt Txt
combined.zip Other
mqpar.xml Xml
uniprot-filtered-organism_Homo_sapiens__Human___9606___AND_review--.fasta Fasta
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Publications

Proteomic Changes of Activated Hepatic Stellate Cells.

Schinagl Maximilian M   Tomin Tamara T   Gindlhuber Juergen J   Honeder Sophie S   Pfleger Raphael R   Schittmayer Matthias M   Trauner Michael M   Birner-Gruenberger Ruth R  

International journal of molecular sciences 20211126 23


Hepatic stellate cells (HSC) are the major cellular drivers of liver fibrosis. Upon liver inflammation caused by a broad range of insults including non-alcoholic fatty liver, HSC transform from a quiescent into a proliferating, fibrotic phenotype. Although much is known about the pathophysiology of this process, exact cellular processes which occur in HSC and enable this transformation remain yet to be elucidated. In order to investigate this HSC transformation, we employed a simple, yet reliabl  ...[more]

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